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De Novo Aneurysm Risk After Aneurysmal Subarachnoid Hemorrhage in Young Survivors

The study was approved by the Swedish Ethical Review Authority (Dnr 2012÷967−31÷3, with subsequent amendments including Dnr 2023−07233−02 and Dnr 2025−01810−02) with a waiver of informed consent. Reporting follows Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guidelines.7

This population-based cohort study included all residents of the Stockholm region younger than 40 years with saccular aSAH between January 1, 1967, and December 31, 2014. Cases were identified through the prospectively maintained Stockholm Intracranial Aneurysm Register, cross-linked with the Swedish Cause of Death Register8 and National Patient Register9 using codes from the relevant International Classification of Diseases. Sweden organizes neurosurgical care through 6 regional centers with defined catchment areas precluding referral bias, ensuring all regional residents were captured regardless of treating hospital or place of death, including prehospital deaths ascertained through mandatory autopsy. Capture-recapture analysis estimated case ascertainment completeness at 97.7%. All cases were manually verified against original medical records and national register data (eMethods 1 in Supplement 1).

Eligibility required ruptured saccular aneurysm confirmed by concurrent 4-vessel cerebral angiography and availability of original index imaging for de novo validation. Nonsaccular etiologies (arteriovenous malformation–related, dissecting, mycotic, or Moyamoya-associated aneurysms) were excluded. During 1967 to 1986, regional neurosurgical care was provided at Karolinska University Hospital (Karolinska) and Stockholm South General Hospital (SGH).10 The original-imaging requirement for de novo validation excluded a substantial proportion of SGH patients from this period, as films were generally not retained after the department’s closure in 1987; SGH patients with preserved imaging were eligible under identical criteria (eMethods 1 and eTable 6 in Supplement 1). Patients treated at other neurosurgical centers but followed up in the Stockholm region with original imaging available were also eligible.

Earth’s Core Is Leaking All Sorts of Materials That Have Been Trapped Since Our Planet’s Birth

Our early Earth was a heavy metal album cover: a molten ball covered in a global lava ocean, spewing lethal gases while being pelted by the flaming space-rocks of our Solar System’s violently chaotic afterbirth.

Over the next 4.5 billion years of hectic cosmo-geological time, it has settled down a bit, allowing humans, lemurs, and others to emerge.

A vision of this hellish ancient reality remains, (hopefully) never to be glimpsed by human eyes: our molten metallic core, blazing about as hotly as the surface of the Sun.

Unmasking “zombie cells” in aging tissue with an AI-powered barcode

Artificial intelligence may transform molecular biology not by always providing the correct answer, but by exploring mechanistic possibilities unconstrained by the assumptions that shape expert thinking. Its greatest contribution may be exposing the intellectual blind spots of scientists, while experimental validation remains the ultimate arbiter of truth.

Challenging Anatomic and Pathologic Features for Transcatheter Aortic Valve Replacement Planning

Blanke P, Weir-McCall JR, Achenbach S, et al. Computed Tomography Imaging in the Context of Transcatheter Aortic Valve Implantation (TAVI)/Transcatheter Aortic Valve Replacement (TAVR): An Expert Consensus Document of the Society of Cardiovascular Computed Tomography. JACC Cardiovasc Imaging 2019;12:1–24.

Crossref.

The Neuro Revolution Is Dawning. Are We Ready?

Georgia Tech researchers are exploring new frontiers in neuroethics: to ensure that emerging neurotechnologies can be used for the good of all and to ensure that we won’t inadvertently relinquish crucial human rights which have yet to be legally defined.

[ https://news.research.gatech.edu/feature/neuro-society](https://news.research.gatech.edu/feature/neuro-society)

As neuroscience and neurotechnology accelerate, Georgia Tech researchers are examining what a neuro-connected future could mean for society and for humanity itself.

ASCL1 and OLIG2 Expression Dynamics Control Glial Cell Fate and Regional Diversity in the Dorsal Forebrain

Gliogenesis is a multistep process in which glial progenitors are specified into migrating and proliferating precursor cells that subsequently differentiate into mature astrocytes and oligodendrocytes. How these developmental processes are coordinated to generate the diverse glial lineages across gray matter (GM) and white matter (WM) remains poorly understood. Here, we show that the basic-helix-loop-helix (bHLH) transcription factor ASCL1 serves as a direct mechanistic link between these processes in the dorsal forebrain. Notably, ASCL1 is dynamically expressed in glial progenitor cells, initiating in the ventricular zone (VZ), peaking in the intermediate zone (IZ), but is downregulated once glial cells enter the cortical plate. Lineage tracing of ASCL1+ progenitors demonstrates that they subsequently co-express OLIG2 to generate both astrocytes and oligodendrocytes in an “outside-in” pattern starting from the upper cortex inward to the corpus callosum, the opposite pattern of neurogenesis. ASCL1 gain-of-function combined with OLIG2 loss-of-function reveals that sustained levels of ASCL1 are essential to induce sufficient levels of OLIG2 required to specify oligodendrocyte precursor cell (OPC) fate. Interestingly, a persistent ASCL1 expression also maintains OPCs in an undifferentiated, pre-neoplastic state into postnatal stages, in part by suppressing their differentiation into postmitotic oligodendrocytes. Together, these findings establish ASCL1 as a key regulator of the spatiotemporal order of glial lineage diversity in cortical GM and callosal WM, and highlight ASCL1 dysregulation as an underlying developmental mechanism in the pathogenesis of gliomas.

Significance statement The brain relies on macroglia to form the blood-brain-barrier, insulate nerve fibers, and regulate neuronal signaling; yet how these cell types are generated remains poorly understood. This study shows that the timing and levels of two key regulatory proteins, ASCL1 and OLIG2, function together to guide immature glial cells through distinct stages of development. Notably, we show that brief ASCL1 activity followed by sustained ASCL1 and OLIG2 levels coordinate when glial cells form, the cell type they become, and where they migrate to reside in the cerebral cortex. By revealing the developmental program underlying the generation of glial cell diversity, this study provides a framework for understanding how glial-related neurological diseases and cancer arise in the brain.